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Avaliação da resposta imune celular na coinfecção por HIV e LeishmaniaGois, Luana Leandro January 2011 (has links)
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Previous issue date: 2011 / Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, Bahia, Brasil / A Leishmania é considerada um patógeno oportunista em indivíduos infectados pelo HIV. Os
mecanismos imunopatogênicos pelos quais o HIV e a Leishmania interagem não estão bem
esclarecidos. Assim como, não está definido de que forma a infecção pelo HIV provoca
alterações na resposta imune celular específica à Leishmania, o que conduz às apresentações
atípicas e disseminadas da leishmaniose descritas nos pacientes coinfectados. O objetivo desta
dissertação foi avaliar a resposta imune celular dos pacientes coinfectados por HIV e
Leishmania, mais especificamente avaliar a resposta Th1 e perfil das subpopulações de
linfócitos T de memória. Para tal, foi avaliada a resposta linfoproliferativa ao antígeno solúvel
de Leishmania (SLA) e a proporção das subpopulações de memória central e efetora dos
linfócitos T CD4+ específicos para Leishmania por citometria de fluxo. O índice de divisão
celular dos linfócitos T CD4+ e CD8+ após o estímulo com SLA dos pacientes coinfectados
foi estatisticamente menor em comparação com os pacientes infectados apenas por
Leishmania. A resposta proliferativa dos linfócitos T CD4+ ao SLA foi observada em 25 %
dos pacientes coinfectados, enquanto que em 12 % dos pacientes coinfectados foi observada
proliferação dos linfócitos T CD8+ em resposta ao SLA. Entretanto, em todos os pacientes
infectados apenas por Leishmania foi notada a linfoproliferação em resposta ao SLA. As
proporções de linfócitos T CD4+ de memória central e efetora específicos para Leishmania
foram similares entre os pacientes coinfectados e os pacientes infectados apenas por
Leishmania. Entretanto, o número absoluto dos linfócitos T CD4+ de memória central e
efetora foi significantemente menor nos pacientes coinfectados em comparação aos pacientes
infectados apenas por Leishmania. Os resultados demonstram um prejuízo funcional na
imunidade celular específica dos pacientes coinfectados. / The Leishmania is opportunistic pathogens in HIV-1-infected individuals. The
immunopathogenic mechanisms by which HIV and Leishmania adversely affect each other
are unclear. Furthermore, the impact of HIV-1 on Leishmania-specific cellular immune
response leads to atypical and disseminated lesions as described in co-infected patients. The
aim of this dissertation is to evaluate the cellular immune response of HIV and Leishmania
co-infected patients, specifically to evaluate the profile Th1 and the memory CD4+ T-cell
subset. The proliferative response of CD4+ and CD8+ T-cells to soluble Leishmania antigens
(SLA) and the frequency memory Leishmania-specific CD4+ T-cell were performed flow
cytometry. The median of cell division index of CD4+ and CD8+ T-cells after stimulation with
SLA from co-infected patients was significantly lower than in patients infected Leishmania
solely. A proliferative response of CD4+ T-cells after stimulation with SLA was observed in
25 % of co-infected patients, while in 12 % of co-infected patients had a proliferative
response in the CD8+ T-cells to SLA. In contrast, both CD4+ and CD8+ T-cells subset from all
patients infected with Leishmania solely proliferated in response to SLA. The proportion of
Leishmania-specific central and effector memory CD4+ T-cells were similar between the coinfected
patients and patients infected Leishmania solely. However, the median of absolute
number of Leishmania-specific central and effector memory CD4+ T-cells from co-infected
patients were significantly lower compared to patients infected Leishmania solely. These
results demonstrate the impairment in cellular immune response.
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Care of HIV-infected children before and after antiretroviral therapy initiation in West Africa : contribution towards the development of a multi-state model / La prise en charge du VIH pédiatrique avant et après traitement antirétroviral en Afrique de l’Ouest : contribution au développement d’une modélisation multi-étatsDesmonde, Sophie 20 December 2013 (has links)
L’accès aux interventions de la prévention de la transmission mère-enfant (PTME) est limité en Afrique de l’Ouest et les mères infectées continuent de transmettre le virus à leurs enfants. D’importantes questions sur le diagnostic et traitement antirétroviral (TAR) précoce pour les enfants dans les pays à ressources-limitées restent sans réponses. La simulation est un outil utile qui permet d’intégrer toutes les données disponibles et de projeter à long terme les retombées cliniques et économiques de l’infection à VIH pédiatrique et informer les politiques de santé. Bien que les modèles de simulation soient mathématiquement sophistiqués, l’utilité des études basées sur la simulation dépend de la qualité des données de départ. L’objectif principal de ce travail était de fournir des données originales et récentes sur la mortalité, morbidité sévère et recours aux soins chez les enfants infectés par le VIH suivis dans des programmes de soins, avant et après initiation du TAR, dans le contexte du passage à l’échelle du TAR depuis 2004 en Afrique de l’Ouest. Nos résultats font ressortir un taux de mortalité comparable à d’autres études, atteignant 5.5% après 18 mois de suivi dans une cohorte d’enfants non traités par TAR, inclus à un âge médian de 5 ans. Les taux de morbidité sévère étaient élevés chez les enfants non traités mais aussi traités. Nous avons rapportés qu’une hospitalisation sur trois était provoquée par une morbidité infectieuse, évitable par une prophylaxie par cotrimoxazole, une intervention simple et efficace qui n’est toujours pas accessible à tous en Afrique de l’Ouest. Nous avons également observé un recours aux soins importants associé à la morbidité sévère. Cependant, parmi les enfants non traités, comme les traités, le recours aux soins était plus faible parmi les enfants les plus immunodéprimés. Le principal obstacle aux recours aux soins était le coût associé pour les familles. Enfin, les enfants qui initiaient un TAR l’initiaient trop tard, à un stade trop avancée de la maladie pour une restitution immunitaire pour âge ; la probabilité de rattraper une immunité normale était encore plus faible chez les enfants âgés > 5 ans comparé aux plus jeunes. Globalement, ce travail met en avant la nécessité de la mise en place de stratégies de diagnostic et traitement précoce. Optimiser le parcours de soins ainsi implique des interventions à de nombreux niveaux du système de soins et aucune approche unique ne pourra être efficace. De plus, les coûts liés à une prise en charge à vie devront être estimés dans un contexte où le VIH devient une maladie chronique engendrant un plus gros recours aux soins. Intégrer ces données dans un modèle de simulation permettra d’informer les politiques de santé et les soignants afin d’identifier les stratégies les plus efficaces et coût-efficaces pour le diagnostic, le traitement et le suivi à long terme de l’enfant infecté par le VIH dans les pays à ressources limitées. / Access to prevention of mother-to-child transmission (PMTCT) interventions is limited in West Africa and mothers continue to transmit HIV disease to their children. Important questions on early HIV diagnosis and early antiretroviral therapy (ART) for children in resource-limited settings remain unanswered. Computer simulation models can provide helpful information to project long-term patient outcomes and inform health policy. Although simulation models are computationally sophisticated, the usefulness of the results of modelling studies depends on the quality and accuracy of the data on which they are based. The main objective of the following work was to provide accurate and up-to-date data on mortality, severe morbidity and healthcare resource utilisation in HIV-infected children enrolled in care, before and after ART initiation in the context of the access to ART roll-out since 2004 in West Africa. Our findings suggest mortality rates comparable to those of other studies, reaching 5.5% by 18 months of follow-up in children enrolled in cohorts at a median age of 5 years who had not yet initiated ART. Severe morbidity rates were high, in both ART-treated and untreated children. We found that one hospitalisation in three was caused by an infectious disease, avoidable by cotrimoxazole prophylaxis, a simple and efficient intervention that is still not accessible to all in West Africa. We also reported substantial rates of healthcare resource utilisations associated with this severe morbidity. However, in both untreated and ART-treated children, healthcare resource utilisation was lower in the sickest, most immunodeficient children. Access to healthcare remains limited and one of the explanations we put forward are the costs borne by the families. Finally, children on ART remain initiated at a too late stage to be able to restore normal immunity for age; this is even less likely in those who initiated ART after 5 years compared to younger children. Overall, this work underlines the need for an effective early HIV diagnosis and treatment. Optimising this requires interventions at multiple levels of the healthcare system and no single approach is likely to be effective. Furthermore, lifetime treatment costs will need to be assessed as HIV becomes a chronic disease leading to greater healthcare resource utilisation. Integrating these data in computer simulation models will assist healthcare providers and policy-makers to identify the most effective and cost-effective strategies for diagnosis, treatment and monitoring of paediatric HIV in low income countries.
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